A crucial role in the efforts of prevention of end-organ damage plays the renin angiotensin system (RAS) due its dual role on salt and water homeostasis (blood pressure) and the vascular response to injury. The increased mechanical strain on the vasculature at a higher BP can cause injury to the endothelial wall. Activation of the RAS increases BP and stimulates a local inflammatory response to repair the injury. Long-term or repeated response to injury leads to endothelial dysfunction and microvascular damage (12), and hence end-organ damage. Therefore increasing evidence is not suppressing, that antihypertensive medications which inhibit the RAS may provide incremental end-organ protection.